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Published online 14 November 2001. The study of families with inherited cardiac arrhythmias has established the genetic basis of primary arrhythmogenic disorders. Culprit genes have been identified for familial causes of ventricular arrhythmias, including the long QT syndrome, Brugada syndrome, and polymorphic ventricular tachycardia. Thus far, the genetic defects leading to these disorders have been shown to affect ion channel proteins (‘channelopathies’) or in the case of polymorphic ventricular tachycardia, the cardiac ryanodine receptor which is known to be involved in intracellular calcium handling. Recently, we identified genetic mutations in the gene encoding for the gamma 2 regulatory subunit (PRKAG2) of AMP-activated protein kinase as responsible for the familial syndrome of ventricular preexcitation, atrial fibrillation, and conduction defects. The novel association of this protein with abnormal atrioventricular connections and supraventricular arrhythmias offers a new perspective on heart development and arrhythmogenesis.

AMP-activated protein kinase and familial Wolff–Parkinson–White syndrome: new perspectives on heart development and arrhythmogenesis